Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: A randomized controlled trial
Identifieur interne : 001073 ( Istex/Corpus ); précédent : 001072; suivant : 001074Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: A randomized controlled trial
Auteurs : Yoshihiro Sato ; Jun Iwamoto ; Tomohiro Kanoko ; Kei SatohSource :
- Movement Disorders [ 0885-3185 ] ; 2006-07.
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- KwdEn :
Abstract
Incidence of a fracture, particularly in the hip joint, is high in elderly women with Parkinson's disease (PD), and this is due to the immobilization‐induced bone resorption and vitamin D deficiency with reduced bone mineral density (BMD). The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2‐year follow‐up period was studied. At baseline, both groups of patients had low BMD with high levels of serum‐ionized calcium and urinary deoxypyridinoline (D‐Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10–0.85). The number of hip fracture per 1,000 patient‐years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D‐Pyr levels decreased significantly during the follow‐up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (P < 0.01). Treatment with alendronate and vitamin D2 increases BMD in elderly women with PD and leads to the prevention of hip fractures. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.20825
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ISTEX:B32FD1A39905B841FDF0E6F60A13D417FED9580FLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: A randomized controlled trial</title><author><name sortKey="Sato, Yoshihiro" sort="Sato, Yoshihiro" uniqKey="Sato Y" first="Yoshihiro" last="Sato">Yoshihiro Sato</name><affiliation><mods:affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan</mods:affiliation></affiliation></author><author><name sortKey="Iwamoto, Jun" sort="Iwamoto, Jun" uniqKey="Iwamoto J" first="Jun" last="Iwamoto">Jun Iwamoto</name><affiliation><mods:affiliation>Department of Sports Medicine, Keio University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kanoko, Tomohiro" sort="Kanoko, Tomohiro" uniqKey="Kanoko T" first="Tomohiro" last="Kanoko">Tomohiro Kanoko</name><affiliation><mods:affiliation>Department of Rehabilitation Medicine, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Satoh, Kei" sort="Satoh, Kei" uniqKey="Satoh K" first="Kei" last="Satoh">Kei Satoh</name><affiliation><mods:affiliation>Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:B32FD1A39905B841FDF0E6F60A13D417FED9580F</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1002/mds.20825</idno><idno type="url">https://api.istex.fr/document/B32FD1A39905B841FDF0E6F60A13D417FED9580F/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001073</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: A randomized controlled trial</title><author><name sortKey="Sato, Yoshihiro" sort="Sato, Yoshihiro" uniqKey="Sato Y" first="Yoshihiro" last="Sato">Yoshihiro Sato</name><affiliation><mods:affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan</mods:affiliation></affiliation></author><author><name sortKey="Iwamoto, Jun" sort="Iwamoto, Jun" uniqKey="Iwamoto J" first="Jun" last="Iwamoto">Jun Iwamoto</name><affiliation><mods:affiliation>Department of Sports Medicine, Keio University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kanoko, Tomohiro" sort="Kanoko, Tomohiro" uniqKey="Kanoko T" first="Tomohiro" last="Kanoko">Tomohiro Kanoko</name><affiliation><mods:affiliation>Department of Rehabilitation Medicine, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Satoh, Kei" sort="Satoh, Kei" uniqKey="Satoh K" first="Kei" last="Satoh">Kei Satoh</name><affiliation><mods:affiliation>Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-07">2006-07</date><biblScope unit="vol">21</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="924">924</biblScope><biblScope unit="page" to="929">929</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">B32FD1A39905B841FDF0E6F60A13D417FED9580F</idno><idno type="DOI">10.1002/mds.20825</idno><idno type="ArticleID">MDS20825</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>alendronate</term><term>hip fracture</term><term>hypercalcemia</term><term>vitamin D</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Incidence of a fracture, particularly in the hip joint, is high in elderly women with Parkinson's disease (PD), and this is due to the immobilization‐induced bone resorption and vitamin D deficiency with reduced bone mineral density (BMD). The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2‐year follow‐up period was studied. At baseline, both groups of patients had low BMD with high levels of serum‐ionized calcium and urinary deoxypyridinoline (D‐Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10–0.85). The number of hip fracture per 1,000 patient‐years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D‐Pyr levels decreased significantly during the follow‐up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (P < 0.01). Treatment with alendronate and vitamin D2 increases BMD in elderly women with PD and leads to the prevention of hip fractures. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Yoshihiro Sato MD</name><affiliations><json:string>Department of Neurology, Mitate Hospital, Tagawa, Japan</json:string></affiliations></json:item><json:item><name>Jun Iwamoto MD</name><affiliations><json:string>Department of Sports Medicine, Keio University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Tomohiro Kanoko BSc</name><affiliations><json:string>Department of Rehabilitation Medicine, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</json:string></affiliations></json:item><json:item><name>Kei Satoh MD</name><affiliations><json:string>Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>alendronate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hip fracture</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hypercalcemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>vitamin D</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Incidence of a fracture, particularly in the hip joint, is high in elderly women with Parkinson's disease (PD), and this is due to the immobilization‐induced bone resorption and vitamin D deficiency with reduced bone mineral density (BMD). The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2‐year follow‐up period was studied. At baseline, both groups of patients had low BMD with high levels of serum‐ionized calcium and urinary deoxypyridinoline (D‐Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10–0.85). The number of hip fracture per 1,000 patient‐years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D‐Pyr levels decreased significantly during the follow‐up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (P > 0.01). 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The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2‐year follow‐up period was studied. At baseline, both groups of patients had low BMD with high levels of serum‐ionized calcium and urinary deoxypyridinoline (D‐Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10–0.85). The number of hip fracture per 1,000 patient‐years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D‐Pyr levels decreased significantly during the follow‐up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (P < 0.01). Treatment with alendronate and vitamin D2 increases BMD in elderly women with PD and leads to the prevention of hip fractures. © 2006 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>alendronate</term></item><item><term>hip fracture</term></item><item><term>hypercalcemia</term></item><item><term>Parkinson's disease</term></item><item><term>vitamin D</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-07-29">Received</change><change when="2005-09-23">Registration</change><change when="2006-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/B32FD1A39905B841FDF0E6F60A13D417FED9580F/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2‐year follow‐up period was studied. At baseline, both groups of patients had low BMD with high levels of serum‐ionized calcium and urinary deoxypyridinoline (D‐Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10–0.85). The number of hip fracture per 1,000 patient‐years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D‐Pyr levels decreased significantly during the follow‐up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (<i>P</i> < 0.01). Treatment with alendronate and vitamin D2 increases BMD in elderly women with PD and leads to the prevention of hip fractures. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: A randomized controlled trial</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Alendronate and Vitamin D2</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Alendronate and vitamin D2 for prevention of hip fracture in Parkinson's disease: A randomized controlled trial</title></titleInfo><name type="personal"><namePart type="given">Yoshihiro</namePart><namePart type="family">Sato</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan</affiliation><description>Correspondence: Department of Neurology, Mitate Hospital, 3237 Yugeta, Tagawa 826‐0041, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jun</namePart><namePart type="family">Iwamoto</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Sports Medicine, Keio University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomohiro</namePart><namePart type="family">Kanoko</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Department of Rehabilitation Medicine, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kei</namePart><namePart type="family">Satoh</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2006-07</dateIssued><dateCaptured encoding="w3cdtf">2005-07-29</dateCaptured><dateValid encoding="w3cdtf">2005-09-23</dateValid><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">3</extent><extent unit="references">23</extent><extent unit="words">4068</extent></physicalDescription><abstract lang="en">Incidence of a fracture, particularly in the hip joint, is high in elderly women with Parkinson's disease (PD), and this is due to the immobilization‐induced bone resorption and vitamin D deficiency with reduced bone mineral density (BMD). The objective of this study was to address the possibility that treatment with alendronate and vitamin D2 may reduce the incidence of hip fractures in elderly women with PD. PD patients were randomly assigned to daily treatment with 5 mg alendronate (n = 144) or a placebo combined with 1,000 IU of vitamin D2 (n = 144) and followed for 2 years. Incidence of hip fractures in the two patient groups during the 2‐year follow‐up period was studied. At baseline, both groups of patients had low BMD with high levels of serum‐ionized calcium and urinary deoxypyridinoline (D‐Pyr). Hip fractures occurred in 14 patients in the placebo group and 4 in the alendronate group. The relative risk for hip fractures in the alendronate group as compared with the placebo group was 0.29 (95% CI, 0.10–0.85). The number of hip fracture per 1,000 patient‐years was 14 and 49 for the alendronate and placebo groups, respectively. In the alendronate group, serum calcium and urinary D‐Pyr levels decreased significantly during the follow‐up period, while the levels in the placebo group were increased. BMD increased by 3.1% in the alendronate group and decreased by 2.8% in the placebo group (P < 0.01). Treatment with alendronate and vitamin D2 increases BMD in elderly women with PD and leads to the prevention of hip fractures. © 2006 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>alendronate</topic><topic>hip fracture</topic><topic>hypercalcemia</topic><topic>Parkinson's disease</topic><topic>vitamin D</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>924</start><end>929</end><total>6</total></extent></part></relatedItem><identifier type="istex">B32FD1A39905B841FDF0E6F60A13D417FED9580F</identifier><identifier type="DOI">10.1002/mds.20825</identifier><identifier type="ArticleID">MDS20825</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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